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Aspirin-exacerbated respiratory disease: evaluation and management.

The clinical syndrome of aspirin-exacerbated respiratory disease (AERD) is a condition where inhibition of cyclooxygenase-1 (COX-1) induces attacks of upper and lower airway reactions, including rhinorrhea and varying degrees of bronchospasm and laryngospasm. Although the reaction is not IgE-mediated, patients can also present with anaphylactic hypersensitivity reactions, including hypotension, after exposure to COX-1 inhibiting drugs. All patients with AERD have underlying nasal polyps and intractable sinus disease which may be difficult to treat with standard medical and surgical interventions.

This review article focuses on the management of AERD patients with a particular emphasis on aspirin desensitization and continuous treatment with aspirin.

Eosinophilic cationic protein: is it useful in assessing control of childhood asthma?

This study evaluated peripheral eosinophil and serum eosinophilic cationic protein (s-ECP) levels as markers of asthma control.

A total of 38 children with asthma (16 controlled and 22 partially controlled) were compared with 16 age- and sex-matched healthy children. Total asthma cases had higher eosinophil counts and s-ECP levels than healthy children and partially controlled asthmatics had significantly higher levels of both markers than controlled asthmatics. Controlled asthma cases showed non-significant changes in both parameters versus healthy children.

A negative correlation was noted between degree of asthma control and both eosinophil counts and s-ECP levels (r = -0.60 and -0.75 respectively). s-ECP as well as peripheral eosinophil count may be helpful in the assessment of asthma control.

Can beta-blockers be used for people with COPD?

Chronic obstructive pulmonary disease (COPD) is a disabling condition characterised by largely irreversible airflow obstruction, and affects over 3 million people in the UK. Due in large part to shared risk factors - notably smoking - patients with COPD often also have cardiovascular diseases, such as ischaemic heart disease and heart failure.

In these conditions, beta-blockers are valuable management options with proven benefits on symptoms and mortality. Historically, however, clinicians have been reluctant to prescribe beta-blockers for patients with co-existing COPD, due to fear of provoking bronchoconstriction. Moreover, such patients have typically been excluded from trials of beta-blockers, raising additional concerns about the basis for treating them with these drugs. However, withholding beta-blocker therapy might lead to suboptimal treatment for cardiovascular disease among these patients.

Here we review the efficacy and safety of beta-blockers in patients with COPD.

Adherence to treatment guidelines and long-term survival in hospitalized patients with chronic obstructive pulmonary disease.

Adherence to treatment guidelines in chronic obstructive pulmonary disease (COPD) has been shown to be less than optimal over the COPD continuum. This retrospective study aimed to assess the implementation of COPD guidelines and potential association with long-term mortality in patients with COPD.

Methods  All consecutive patient discharges in the period of February 2002-June 2007 from the University Clinic of Pulmonary and Allergic Diseases Golnik, Slovenia, were screened for a primary discharge diagnosis of COPD.

Results  Data on 1185 patients (mean age 70 ± 9 years, 72% men, 64% GOLD stage III/IV) were analysed. In the discharge letters 62% of patients had three or more drugs prescribed; 3% had no regular prescription. Most patients were discharged with short-acting (91%) and long-acting β2-agonists (LABAs, 65%) and inhaled corticosteroids (61%), and 23% received long-term oxygen therapy. Prescription rates of LABAs, tiotropium and inhaled corticosteroids increased over the disease continuum (P < 0.001). In total, 48% of patients died during a median follow-up of 1149 days. Deceased patients had been less often treated with LABAs, inhaled corticosteroids and tiotropium. In multivariate Cox proportional-hazards analysis, advanced age, current smoking status, lower body mass index, longer hospital stay and cancer were associated with higher mortality (P < 0.05 for all), and inhaled corticosteroids predicted lower mortality (hazard ratio 0.72, 95% confidence interval 0.55-0.94).

Conclusion  Implementation of guideline-recommended therapy was not optimal, particularly in patients who died during follow-up. The high long-term mortality calls for careful risk assessment and appropriate adherence to treatment guidelines.

The role of augmentation therapy in alpha-1 antitrypsin deficiency.

Since the recognition of alpha-1 antitrypsin deficiency (A1ATD) in 1963, interest in this condition has increased dramatically. A1ATD is now recognized as the only known genetic condition that leads to emphysema/chronic obstructive pulmonary disease (COPD) in many individuals with the condition. Augmentation therapy with plasma-derived alpha-1 antitrypsin (A1AT) was first introduced in 1987.

Objectives and scope: To review current evidence on the efficacy, tolerability and biochemical composition of commercially available A1AT augmentation therapies. Literature was sought via electronic searching of bibliographic databases (MEDLINE) and other sources. No language or time period settings were applied. This is a narrative, descriptive review rather than a formal, systematic review.

Findings: Evidence of the therapeutic efficacy of A1AT augmentation therapy is beginning to accumulate, although further randomized, controlled trials are necessary. Clinical studies have reported reduced rates of lung function decline in COPD patients who received augmentation therapy, and significant benefit is seen in patients with forced expiratory volume in 1 second initially in the range of 35-49% of predicted normal. Augmentation therapy has also been shown to decrease the frequency of severe COPD exacerbations and to significantly increase survival rate. Biochemical studies have convincingly demonstrated that weekly intravenous infusion of each of the available plasma-derived A1AT preparations maintains serum A1AT levels above the putative protective threshold. Augmentation therapy with intravenous A1AT is generally well tolerated and long-term therapy in patients with severe A1ATD and pulmonary emphysema is feasible. Differences in the purification processes of available A1AT products are reflected in their relative purities and heterogeneities (abundance of A1AT isoforms), although the commercially available preparations are bioequivalent. Further studies are required to clarify whether variations in biochemical composition of purified A1AT are clinically important.

Conclusion: Intravenous augmentation therapy with A1AT currently represents the only viable and specific treatment option for patients with A1ATD.

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